?/ANTI-? COMPLEXES: STAPHYLOCOCCAL AUREUS PHAGE G1 ORF67

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 细菌的转录依赖于对生存至关重要的初级(第1组)。此外，大多数细菌含有替代的S，它控制调节对环境提示的调节。活性的调节是细菌对环境做出反应的主要机制。许多替代的S受反转录因子的调节。尽管S的结构保持保守，但反的S在结构和功能上是多样化的，作为关键反应元件，通过替代的S感知环境提示并向核心转录装置发送信号。 除了细胞抗因子对功能的调节外，许多噬菌体还进化出巧妙的机制来抑制和/或调节宿主转录装置。革兰氏阳性病原体金黄色葡萄球菌(SAU)的主要靶标是抑制细菌生长的噬菌体蛋白。噬菌体G1 ORF67在高通量筛选中被鉴定为与Sau？A(？A4)的C-末端结构域(结构域4)结合的转录抑制物。我们的目标是确定G1ORF67与SauA4的共晶结构，并探讨ORF67抑制Sau转录的作用机制及其在噬菌体G1生物学中的作用。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Bacterial transcription depends on a primary (group 1) ¿ that is essential for viability. In addition, most bacteria contain alternative ¿'s that control regulons in response to environmental cues. Regulation of ¿ activity is a major mechanism by which bacteria respond to their environment. Many alternative ¿'s are regulated by anti-¿ factors. Despite the structural conservation of ¿'s, anti-¿'s are structurally and functionally diverse, serving as the key response elements to sense and signal environmental cues to the core transcriptional apparatus via the alternative ¿'s. In addition to modulation of ¿ function by cellular anti-¿ factors, many bacteriophages have evolved ingenious mechanisms to inhibit and/or appropriate the host transcription apparatus. The primary ¿ (¿A) of the gram-positive pathogen Staphylococcus aureus (Sau) is targeted by phage proteins that inhibit bacterial growth. Phage G1 ORF67 was identified in a high-throughput screen as a transcriptional inhibitor that binds to the C-terminal domain (domain 4) of Sau ¿A (¿A4). Our goal is to determine the co-crystal structure of G1 ORF67 with Sau ¿A4, and to explore the functional mechanism through which ORF67 inhibits Sau transcription as well as it's role in phage G1 biology.